Type of cancer | Dose range | Cell line | Target | Pathway | Function | Refs. |
---|---|---|---|---|---|---|
In vivo studies | ||||||
Breast cancer (BCa) | 50 mg/kg, 10–200 mg/L | MCF-7/DOX, MCF-7, MDA-MB-231 | Caspase-3, P70S6K | PI3K/AKT/mTOR | RVT via inhibiting PI3K/AKT/ mTOR pathway could play a role in DOX resistance in breast neoplasm | [90] |
Papillary Thyroid cancer (PTC) | 30 mg/kg 50 μM | KTC-1,TPC-1 | Caspase-3/8/9, Bax, Bcl-xl, Mcl-1, p70S6K | PI3K/AKT/mTOR | RVT via the PI3K/AKT/mTOR pathway could promote the anti-tumor effects of rapamycin in papillary thyroid cancer | [89] |
Glioblastoma multiforme (GBM) | 10 mg/kg, 0–20 μM | GICs | IKKα/β, JNK, mTOR, ERK1/2, IκBα p38, MMP-2, Lamin-A, Nestin, GFAP | PI3K/ AKT/NF-κB | RVT via downregulating PI3K/AKT/NF-κB pathway could inhibit invasion of glioblastoma-initiating cells (GICs) | [91] |
In vitro studies | ||||||
Melanoma | 4 μM-18 μM | Human melanoma cell | – | AKT | RVT via dephosphorylation of AKT could overcome resistance to vemurafenib in BRAF-mutated melanoma cells | [86] |
Melanoma | 100 μM | B16 | LC3-l, LC3-ll, Beclin-1, S6K, 4E-BP1 | Ceramide/AKT/mTOR | RVT via the ceramide/AKT/mTOR pathway could trigger protective autophagy in melanoma B16 cells | [87] |
Melanoma | 0–100 μM | B16-F10, A375 | Beclin-1, Caspase-9, P62, LC3II/I | PI3K/ AKT/mTOR | RVT via inhibiting the PI3K/AKT/mTOR pathway could promote autophagy and suppress melanoma growth | [92] |
Pheochromocytoma | 10–1000 μM | PC12 | Caspase-3, iNOS | PI3K, AKT/p38 MAPK | RVT via AKT/p38 MAPK signaling could attenuate apoptosis, and protect neuronal cells from isoflurane-induced inflammation | [93] |
BCa | 10–25 μM | SK-BR-3, MCF7, T47D, MDA-MB-231 | Caspase-7/8, JNK, P38, XIAP, Survivin, Bcl-2 | AKT, HER-2, MAPK | RVT via inhibiting docetaxel-mediated activation of the HER-2/AKT axis could sensitize BCa cells to docetaxel-induced cytotoxicity | [88] |
Bladder cancer | 0–50 μmol/L | T24, 5637, SV-HUC-1 | miR-21, Bcl-2, Caspase-3 | AKT | RVT via miR-21 regulation of the AKT/Bcl-2 pathway could induce apoptosis of bladder cancer cells | [94] |
Chondrosarcoma | 25–100 μM | JJ012, SW1353 | MMP2, MMP9 | PI3K/AKT/MAPK | RVT via regulating the PI3K/AKT/MAPK pathway could inhibit cell proliferation and induce cell apoptosis in chondrosarcoma cells | [95] |
Renal cell carcinoma (RCC) | 0–100 μM | ACHN, A498, HK-2 | N-cadherin, Vimentin, Snail, MMP-2/9, E-cadherin, TIMP-1 | AKT, ERK1/2 | RVT via inactivating the AKT and ERK1/2 pathways could inhibit proliferation and migration in RCC cells | [96] |
Oral cancer | 50 μM | CAR, CAL 27 | LC3-II/I, Caspase-3/9, Atg-5/7/12/14, Beclin-1, Atg16L1, Apaf-1, AIF, Bcl-2, Bax, Bad | AKT/mTOR, AMPK | RVT via the AMPK and AKT/mTOR pathway could regulate autophagy and apoptosis in cisplatin-resistant human oral cancer CAR cells | [97] |
Neuroblastoma (NB) | 10–100 μM | SK-N-SH, SH-SY5Y, SK-N-Be2, SMS-KCNR, NB1691 | GSK3β, IRS-1, Survivin, PP1α, α-tubulin | AKT | RVT via inactivating AKT by increasing PP1α activity could potentiate 2-DG-induced ER stress and NB cell death | [98] |